ABSTRACT
Objective: Adipose derived stem cells [ASCs] secrete numerous neurotrophic factors and cytokines in conditioned medium [CM], which protect neurons by its antioxidative and trophic effects. This research assesses the neuroprotective effect of ASCCM on neurotrophins genes expressions and tyrosine hydroxylase positive [TH+] cell density in male Wistar rats lesioned by 6-hydroxydopamine [6-OHDA]
Materials and Methods: In this experimental study, the groups consisted of lesioned and sham rats with unilateral injections of 20 microg of 6-OHDA neurotoxin and phosphate buffered saline [PBS] into the striatum, respectively. Another groups received intravenous injections of 3×106 cells [ASCs group], 500 microl of CM [ASC-CM group] or medium [alpha-minimal essential medium [alpha-MEM] group]]. All rats underwent evaluations with the rotarod and apomorphine-induced rotation tests at 2, 4, 6, and 8 weeks post-injection. At 8 weeks we sacrificed some of the animals for real-time polymerase chain reaction [PCR] analysis, and evaluation of TH+ cell counts
Results: We observed a significant decrease in contralateral turns to the lesions in the ASCs and ASC-CM groups compared to the neurotoxin lesioned or alpha-MEM groups at 8 weeks post transplantation. Cell and CM- injected rats showed a significant increase of staying on the rotarod compared to the lesion or alpha-MEM groups. Cell and CM-treated rats showed significant increases in the NGF and NT3 genes, respectively, compared with the lesion group. Both treated groups showed significant increases in BDNF gene expression and TH+ cell density
Conclusion: The results suggested that ASCs and ASC-CM protected dopaminergic neurons through the expressions of neurotrophin genes
ABSTRACT
The most important characteristics of PTSD, as an anxiety disorder, are memory disorders and hippocampus is one of the essential structures which plays a critical role in PTSD memory disorders. Traumatic events cause apoptosis and alter the expression of neurotrophic factors in hippocampus. The aim of this study is to evaluate the effects of beta-Estradiol on behavioral responses in PTSD and to study its biochemical and histological mechanisms
We used single prolonged stress [SPS] to develop PTSD in rats. The day after, the rats received electrical foot shock within shock chamber. One week later, in order to test the conditioned fear responses, the freezing behavior of rats were examined for 5 continuous days, as they were placed back in the chamber without any shock. Animals received multiple injections of beta-estradiol or sesame oil, immediately after shock and also on a daily basis through the seven days prior to the test. Hippocampal cell count was implemented after cresyl violet staining. We measured BDNF protein levels by ELISA kit
Main findings of this study confirmed that exaggerated fear response is observed in PTSD group as compared with control group and beta-estradiol administration reduced these exaggerated behavioral responses. We found out that SPS decreases the density of cells in hippocampus and this effect is partly corrected by beta-estradiol; beta-estradiol increased BDNF protein level in hippocampus as compared with PTSD group; BDNF protein level was negatively correlated with freezing response in both SPS+beta-estradiol and SPS+sesame group
The results of this study is consistent with the hypothesis that decreased expression of BDNF contributes to memory impairment in PTSD and up regulation of BDNF by beta-estradiol plays a role in memory treatment
ABSTRACT
The kiwi fruit is known to have dramatic antibacterial, debridement, wound contracture, and angiogenic effects. We propose that kiwifruit is an ideal candidate to enhance the process of wound healing. The present study assessed the effects of wound kiwifruit dressing on cutaneous wound healing in rat. In this experimental study, 30 male Wistar rats were randomly divided into 2 groups of control and kiwifruit group. A full-thickness dermal incision [35 mm length] was made on the right side of the paravertebral region. In the control group, one day after wound induction wounds was dressed with vaseline sterile gauze after normal saline irrigation. In the second group, the wounds were dressed with kiwifruit. Wound healing was evaluated by measuring surface area, percentage of healing, duration of healing, and wound tensile strength. Obtained results showed that the duration of wound healing in kiwi group in comparison with the control was significantly decreased. The amount of wound healing in percent was also significantly different between control and kiwi groups at days 3, 6 [p<0.001], 9 [p<0.05], 12 and 14 [p<0.01]. Comparisons of wound length between control and kiwi group per day showed that kiwi group had significantly lower wound length on day 9, 12, 14 and 16 [p<0.01, 0.001, 0.01 and 0.01, respectively] in comparisons to control group. Also, the wound tensile strength in kiwi group also was significantly greater than the control animals [p<0.01]. We concluded that our study provides some evidence to support the use of kiwi to accelerate wound healing
ABSTRACT
Epilepsy is a neurological disorder which is modulated by different situations and activities. Stress and exercise can have effects on epilepsy; it can reduce or increase its occurrence. We investigated the effect of acute and chronic stress and also regular moderate exercise on the epileptogenesis. In this experimental study, 82 male Wistar rats divided into 7 groups including 2 exercised and stressed categories, received 40 mg/kg pentylenetetrazol [PTZ] every 48 h up to 13 injections. Then the convulsive behavior was rated by Racine scale. The acute stress was applied by a 30 min swimming session in the water with temperatures of 20, 25 and 32[degree]C. The chronic stress was created by repeated sessions of 30 min daily swimming for 5 days in 20[degree]C water. The exercise was a 60 min swimming daily, 5 days a week and for 8 weeks in 25 and 32[degree]C. We demonstrated that the acute stress showed a decrease in kindling threshold, except for the stress in 25[degree]C water which lowered the kindling rate. Similarly, the chronic stress decreased the kindling threshold in the first 5 injections. The exercise did not reduce the kindling threshold but did reduce the kindling rate in both 25 and 32[degree]C water. It is concluded that the swimming stress enhanced the kindling process, but the swimming exercise prevented the kindling. Therefore, the animal learns to cope with the condition in a repeated regular physical activity
ABSTRACT
This research study is an attempt to examine whether the administration of ethanol after memory reactivation would modulate subsequent expression of memory in rats. Additionally, we examined whether this administration alters the density of Cornu Ammonis [CA]1 and CA3 pyramidal and dentate gyrus [DG] granule cells. In this experimental study, adult male Wistar rats [200-300 g] were trained in a fear conditioning system using two 1 second, 0.6 mA shocks with an interval of 180 seconds. Twenty four hours later rats were returned to the chamber for 120 seconds. Immediately after reactivation they were injected with ethanol [0.5, 1, 1.5 mg/ kg] or saline. 1, 7 and 14 days after reactivation, rats were returned to the context for 5 minutes. Seconds of freezing [absence of all movement except respiration] were scored. In the second experiment [described in the previous paragraph], after test 1, animals were anesthetized with sodium pentobarbital and perfused transcardially with phosphate buffer [10 minutes] and 4% paraformaldehyde [15 minutes]. The brains were postfixed in phosphate-buffered 4% paraformaldehyde [24 hours] and 30% sucrose. 10-?m sections were stained with cresyl violet. Data were analyzed by 1-and 2-way ANOVA for repeated measurements by means of SPSS 16.0. Tukey's post hoc test was performed to determine the source of detected significant differences. P <0 .05 were considered significant. Data are presented as mean +/- SEM. Findings from the first experiment indicated that ethanol at a dose of 1.5 mg/kg significantly impaired recall of memory only in the first test. The density of CA1 and CA3 pyramidal and DG granule cells in the ethanol group was decreased [p< 0.01] compared with control group respectively 43.7%, 35.8%, and 37.8. The data demonstrate that ethanol exposure impairs post retrieval processes. Moreover, ethanol decreases the density of CA1, CA3 and DG cells. Presumably it would be a correlation between our behavioral and histological results